Background: Coronary artery spasm (CAS) is a well&#8208;known endothelial dysfunction, and a major cause of vasospastic angina (VSA). The renin&ndash;angiotensin system (RAS) is known to be closely associated with endothelial function. However, there are only a few studies that investigated the impact of RAS inhibitor on long&#8208;term clinical outcomes in VSA patients.

Methods and results: A total of 3349 patients with no significant coronary artery disease, diagnosed with CAS by acetylcholine provocation test were enrolled for this study. Significant CAS was defined as having &ge;70% narrowing of the artery after incremental injections of 20, 50, and 100&nbsp;&mu;g of acetylcholine into the left coronary artery. Patients were divided into 2 groups according to whether the prescription included RAS inhibitor or not (RAS inhibitor group: n=666, non&#8208;RAS inhibitor group; n=2683). To adjust for any potential confounders that could cause bias, propensity score matching (PSM) analysis was performed using a logistic regression model. After PSM analysis, 2 matched groups (524 pairs, n=1048 patients, C&#8208;statistic=0.845) were generated and their baseline characteristics were balanced. During the 5&#8208;year clinical follow&#8208;up, the RAS inhibitor group showed a lower incidence of recurrent angina (8.7% versus 14.1%, P=0.027), total death (0.0% versus 1.3%, P=0.045), and total major adverse cardiovascular events (1.0% versus 4.1%, P=0.026) than the non&#8208;RAS inhibitor group.

jah31629-fig-0002: Cumulative survival curve of the various end points before and after propensity score matching. Figure shows the cumulative incidences of mortality, myocardial infarction, de novo percutaneous coronary intervention (PCI), recurrent angina, and the composite of death, myocardial infarction, or de novo PCI (MACE). The renin–angiotensin system (RAS) inhibitor group (indicated by red) received RAS inhibitors such as angiotensin receptor blockers (ARB) and angiotensin converting enzyme (ACE) inhibitors. The “none” group (indicated by blue) received no RAS inhibitors. HR indicates hazard ratio; MACE, major adverse cardiac events.

Mentions:
Figure 2 showed the incidence of individual and composite cumulative clinical outcomes. There was no difference between the RAS inhibitor group and non‐RAS inhibitor group during the 5‐year follow‐up. However, after a matched analysis, major clinical end points such as the incidence of recurrent angina, total death, and MACE (composed of total death, myocardial infarction, and percutaneous coronary intervention) were significantly lower in the RAS inhibitor group compared with the non‐RAS inhibitor group.

jah31629-fig-0002: Cumulative survival curve of the various end points before and after propensity score matching. Figure shows the cumulative incidences of mortality, myocardial infarction, de novo percutaneous coronary intervention (PCI), recurrent angina, and the composite of death, myocardial infarction, or de novo PCI (MACE). The renin–angiotensin system (RAS) inhibitor group (indicated by red) received RAS inhibitors such as angiotensin receptor blockers (ARB) and angiotensin converting enzyme (ACE) inhibitors. The “none” group (indicated by blue) received no RAS inhibitors. HR indicates hazard ratio; MACE, major adverse cardiac events.

Mentions:
Figure 2 showed the incidence of individual and composite cumulative clinical outcomes. There was no difference between the RAS inhibitor group and non‐RAS inhibitor group during the 5‐year follow‐up. However, after a matched analysis, major clinical end points such as the incidence of recurrent angina, total death, and MACE (composed of total death, myocardial infarction, and percutaneous coronary intervention) were significantly lower in the RAS inhibitor group compared with the non‐RAS inhibitor group.

Background: Coronary artery spasm (CAS) is a well&#8208;known endothelial dysfunction, and a major cause of vasospastic angina (VSA). The renin&ndash;angiotensin system (RAS) is known to be closely associated with endothelial function. However, there are only a few studies that investigated the impact of RAS inhibitor on long&#8208;term clinical outcomes in VSA patients.

Methods and results: A total of 3349 patients with no significant coronary artery disease, diagnosed with CAS by acetylcholine provocation test were enrolled for this study. Significant CAS was defined as having &ge;70% narrowing of the artery after incremental injections of 20, 50, and 100&nbsp;&mu;g of acetylcholine into the left coronary artery. Patients were divided into 2 groups according to whether the prescription included RAS inhibitor or not (RAS inhibitor group: n=666, non&#8208;RAS inhibitor group; n=2683). To adjust for any potential confounders that could cause bias, propensity score matching (PSM) analysis was performed using a logistic regression model. After PSM analysis, 2 matched groups (524 pairs, n=1048 patients, C&#8208;statistic=0.845) were generated and their baseline characteristics were balanced. During the 5&#8208;year clinical follow&#8208;up, the RAS inhibitor group showed a lower incidence of recurrent angina (8.7% versus 14.1%, P=0.027), total death (0.0% versus 1.3%, P=0.045), and total major adverse cardiovascular events (1.0% versus 4.1%, P=0.026) than the non&#8208;RAS inhibitor group.